Long COVID: pathophysiological factors and abnormalities of coagulation, 2023, Simone Turner et al

[Mij]

Highlights

• Long COVID has a multifactorial nature with multiple pathophysiological factors at play.
• Viral factors, host factors (including systemic inflammation, and metabolic, endocrine, and endothelial dysfunction) and downstream impacts (tissue damage from the initial infection, hypoxia, dysbiosis, and autonomic nervous system dysfunction) are key elements underpinning the condition.
• Various factors culminate in the long-term persistence of the disorder (i.e., a thrombotic endothelialitis characterized by endothelial inflammation, hyperactivated platelets, and fibrinaloid microclots).
• We suggest a multipronged treatment agenda for Long COVID treatment trials, incorporating drugs targeting all potential mechanisms, including viral persistence, autoimmunity, immune dysregulation, and gut dysbiosis; with endothelialitis and coagulation abnormalities as two priorities.

Abstract
Acute COVID-19 infection is followed by prolonged symptoms in approximately one in ten cases: known as Long COVID. The disease affects ~65 million individuals worldwide. Many pathophysiological processes appear to underlie Long COVID, including viral factors (persistence, reactivation, and bacteriophagic action of SARS CoV-2); host factors (chronic inflammation, metabolic and endocrine dysregulation, immune dysregulation, and autoimmunity); and downstream impacts (tissue damage from the initial infection, tissue hypoxia, host dysbiosis, and autonomic nervous system dysfunction). These mechanisms culminate in the long-term persistence of the disorder characterized by a thrombotic endothelialitis, endothelial inflammation, hyperactivated platelets, and fibrinaloid microclots. These abnormalities of blood vessels and coagulation affect every organ system and represent a unifying pathway for the various symptoms of Long COVID


https://www.cell.com/trends/endocri...om/retrieve/pii/S1043276023000553?showall=tru

 

[SNT Gatchaman]

Concluding —

There are several potential pathophysiological mechanisms, some of which may be causative and others likely to be epiphenomena. These include viral factors, host factors, and downstream impacts. These mechanisms interact with the vascular endothelium to induce a persistent thrombotic endothelialitis with systemic hypercoagulability.

Ie proposing the observed features of hypercoagulability are downstream, rather than the primary cause.

Co-authors include David Putrino who, aside from publications and interviews, has run an excellent anti-BPS pushback on Twitter; and Ashley Woodcock, who is on council of the Royal College of Physicians and Past President of the British Thoracic Society (OBE for work with CFCs as co-chair of the Montreal Protocol).